Vildone, Romeo A.; Lowman, Robert M.; Hukill, Peter B.; Bloor, Colin M.; Hipona, Florencio A.
April 1967
Angiology;Apr1967, Vol. 18 Issue 4, p204
Academic Journal
Dogs maintained on a regular diet and given 200 or 250 mg/kg triton intravenously at intervals of 5 to 25 days develop a sustained hyperlipemia. The serum triglycerides are the first lipid fractions to rise. Soon thereafter there is a marked rise in the serum cholesterol, with the greater percentage in the free form, and the serum phospholipids. On the higher dose a large number of animals develop intravascular hemolysis, a rise in the serum bilirubin, hemoglobinuric nephrosis, and die within 2 weeks. Animals surviving for from 5 to 9 months develop atherosclerotic lesions in the aorta, coronary, pulmonary, and renal arteries. In one animal myocardial fibrosis and acute myocardial infarction was noted, associated with the severe coronary arterial lesions. In addition, the livers and spleens are enlarged and reveal large numbers of lipid-laden foamy histiocytes suggestive of some unusual storage disease. Similar-appearing foamy histiocytes are also seen in the lymph nodes. The kidneys reveal lipid-laden tubular epithelial cells and lipid-laden macrophages in the interstitial tissue as well as foam cell lesions of the glomeruli. The lesions seen in the present study are briefly compared with the naturally occurring and experimentally induced atherosclerosis in dogs and some of the similarities and differences are mentioned. It is suggested that this technique may serve as a useful experimental model in which to study selected stages of atherosclerosis.


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